Pw1/Peg3 is a potential cell death mediator and cooperates with Siah1a in p53-mediated apoptosis

Proc Natl Acad Sci U S A. 2000 Feb 29;97(5):2105-10. doi: 10.1073/pnas.040378897.

Abstract

Induction of wild-type p53 in mouse fibroblasts causes cell cycle arrest at the G(1) phase, whereas coexpression of p53 and the protooncogene c-myc induces apoptosis. Although p53 transcriptional activity generally is required for both pathways, the molecular components mediating p53-dependent apoptosis are not well understood. To identify factors that could mediate p53-induced cell death, we used a comparative RNA differential display procedure. We have identified Pw1/Peg3 as a gene product induced during p53/c-myc-mediated apoptosis. Pw1/Peg3 is not induced during p53-mediated G(1) growth arrest nor by c-myc alone. Although it is not clear whether the induction of Pw1/Peg3 depends on p53 activity, we show that Pw1/Peg3 interacts with a p53-inducible gene product Siah1a. We demonstrate that coexpression of Pw1/Peg3 with Siah1a induces apoptosis independently of p53 whereas expression of Pw1/Peg3 or Siah1a separately has no effect on cell death. These data suggest that Siah1a and Pw1/Peg3 cooperate in the p53-mediated cell death pathway. Furthermore, we show that inhibiting Pw1/Peg3 activity blocks p53-induced apoptosis. The observation that Pw1/Peg3 is necessary for the p53 apoptotic response suggests a pivotal role for this gene in determining cell death versus survival.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3T3 Cells
  • Animals
  • Apoptosis*
  • Gene Expression
  • Humans
  • Kruppel-Like Transcription Factors
  • Mice
  • Mutagenesis
  • Nuclear Proteins / metabolism*
  • Protein Kinases*
  • Proteins / genetics
  • Proteins / metabolism*
  • Proto-Oncogene Proteins c-myc / metabolism
  • RNA, Antisense
  • RNA, Messenger
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*
  • Ubiquitin-Protein Ligases

Substances

  • Kruppel-Like Transcription Factors
  • Nuclear Proteins
  • PEG3 protein, human
  • Peg3 protein, mouse
  • Proteins
  • Proto-Oncogene Proteins c-myc
  • RNA, Antisense
  • RNA, Messenger
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • Ubiquitin-Protein Ligases
  • seven in absentia proteins
  • Protein Kinases